This invention relates to limiting fluid movement through rents in body tissues, and particularly the invention relates to providing a barrier for fluid movement through a puncture in a membranous tissue such as the dura mater.
For many medical procedures, access to an internal body cavity is made by way of a puncture or other opening in the wall or membrane enclosing the body cavity. Following such a procedure, fluids or fluid-borne materials may pass through the opening or rent, and complications may result. Reliable methods are needed for limiting movement of fluids or fluid-borne materials across openings in membranes enclosing body cavities, to mitigate such complications.
The mammalian brain and spinal cord are closely invested by a membrane termed the pia mater, and are surrounded by a thick inelastic membrane termed the dura mater. A delicate membrane termed the arachnoid envelops the brain and spinal cord between the dura mater and the pia mater. The arachnoid is separated from the pia mater by the so-called intrathecal or subarachnoid space, which is filled with cerebrospinal fluid (“CSF”). The intrathecal space is accessed clinically, usually by a percutaneous needle puncture through the dura, for a wide variety of purposes, including collection of CSF for chemical and cytological analysis and delivery of therapeutic agents. Percutaneous needle puncture through the dura is one of the most common procedures performed in clinical medicine.
Intraspinal administration of anesthetics and analgesics has been performed for over one hundred years; it has in recent years come into increasing use in obstetrics, urology, and orthopedics, and it is now a mainstay of therapy in the rapidly growing field of pain management.
Diagnostic myelography is commonly employed prior to all types of spinal surgery, entailing injection of radiographic contrast material into the intrathecal space. The intrathecal space also provides a depot for administration of chemotherapy, and rapid advances in neurobiology promise a range of new therapies directed at degenerative central nervous system conditions. Diseases such as multiple sclerosis, amyelotrophic lateral sclerosis (Lou Gehrig's disease), Alzheimer's disease, and others, will likely generate increased need for intrathecal access to permit delivery of drugs that may not easily cross the blood-brain barrier.
Headache is the most common complication of dural puncture. The pathogenesis of post dural puncture headache (PDPH) is generally believed to be related to ongoing CSF leak at the site of the dural puncture, although the mechanism of pain is not clear. Low CSF pressure may result in traction on pain sensitive structures, especially where the subject is in the upright position, caused by loss of the cushioning effect of the normal CSF volume. Vascular dilatation in response to low CSF volume may also be a factor, and neurohumeral responses have been implicated as well. Whatever the cause or causes may be, the reported incidence of PDPH ranges from two percent to 75 percent, depending on a variety of epidemiological factors, including the age, gender, and medical condition of the patient. Women are more likely than men to suffer PDPH, and the rate of PDPH is more likely in younger than in older adults; and it is therefore unsurprising that PDPH is a significant problem following spinal anesthesia in the obstetrical population.
Technical factors may play an important role in generation of PDPH, including needle diameter, needle tip configuration, preparation of the skin, and characteristics of injected material. Incidence of PDPH can be reduced by employing a smaller needle (gauge 25 or higher) or by employing a needle having a “pencil tip” with a side port; and some practitioners have recommended orienting the needle in parallel with the dural fibers. The use of small needles as an approach to reducing the occurrence of PDPH is limited by the greater technical difficulty (especially for non-anesthesiologists) of achieving successful dural puncture using smaller needles; and viscosity of some injectates (myelography dies, for example) is too high to permit the use of smaller needles. Even where optimal technique is employed in low risk populations, the incidence of PDPH is reported as five to 20 percent or more in most studies.
The pain due to PDPH is typically severe and long-lasting, and it can be completely disabling in some instances for days to weeks following the dural puncture procedure. PDPH pain can be relieved by maintaining the subject in a supine position, and patients often are confined to bed for the duration of the headache episode. Symptoms associated with PDPH include nausea and vomiting which predisposes the patient to dehydration and impairs the patient's ability to replace lost CSF, prolonging the painful syndrome. Visual disturbances, tinnitus, vertigo, neck stiffness and auditory symptoms all contribute to the disability associated with PDPH. Severe traction on cranial nerves resulting from low CSF pressure can cause significant palsy, particularly of the with cranial nerve. Traction on intracranial vascular structures can result in potentially fatal intracranial hemorrhage, although this complication is rare. The typical onset of PDPH is 24–48 hours after the procedure, with a duration of three to four days, and approximately 75 percent of patients experience resolution of symptoms within seven days after onset, although it is not unusual for PDPH to last for weeks.
Types of treatment for PDPH generally fall into two categories. Nonspecific, supportive therapies including correction of dehydration and administration of analgesics and anti-emetics are generally sufficient for mild PDPH, in conjunction with maintenance of a supine position at bed rest. Corrective therapies include treatments designed to increase CSF volume and obtund the neurohumeral or vascular cause of the headache. Methylxanthenes such as caffeine and theophylline can constrict cerebral venous channels and promote CSF production, and such agents are often sufficient to control mild cases of PDPH.
The definitive treatment for PDPH, however, is to stop the leak by performing an epidural blood patch. This involves drawing 10–20 cc of sterile autologous blood and administering the blood via a standard epidural access procedure at the same spinal level. In theory, the blood patch halts the flow of CSF from the intrathecal space, reversing the pressure gradient from lumbar spine to cranial vault, and pushes the remaining CSF toward the brain to provide support for the intracranial structures, thereby producing immediate relief. The success rate of the dural blood patch in mitigating PDPH is reported as 85–95 percent. Complications from the dural blood patch procedure are unusual, other than mild low back discomfort and stiffness, but there are case reports of subdural hematoma, abscess formation, arachnoiditis, and even blindness following repeat epidural blood patch. Attempts to employ an epidural blood patch prophylactically have uniformly failed to mitigate PDPH. And the epidural blood patch procedure is highly costly from an economic standpoint.
Accordingly, PDPH continues to be a very troublesome complication of otherwise successful intrathecal access by dural puncture, which may have important implications for the patient's post-operative course. For instance, PDPH following cesarean section results in poorer maternal-infant bonding and inability to breast-feed. Diagnostic lumbar puncture is frequently performed for diagnosis of headache, for example to rule out meningitis, and the presence of PDPH may seriously confound efforts and diagnosis. PDPH is very costly in terms of lost days at work and diminished productivity, and additional days of hospitalization, economically burdening the patient and the employer as well as the health care and health insurance systems.
A need persists for a method of reliably preventing PDPH as a complication of dural puncture procedures.